Exercise is supposed to be good for you, good for your heart, right? Then why is that endurance athletes have two to ten times the rate of developing atrial fibrillation compared to “normal” people? Is a little or moderate exercise good but excessive exercise bad? As an endurance athlete (marathons, trail running, long distance mountain and road biking) who has permanent atrial fibrillation (AF) I would certainly like to understand “WHY?”

The studies aren’t large, and male athletes predominate – but it is clear that endurance athletes have, as mentioned above – 2 to 10 times the likelihood of developing AF. It is not actually known why but it is thought that ectopic atrial beats, chronic inflammation, and larger atrial size are all risk factors.

Personally – the story checks out – I started having runs of “premature atrial contractions” years before ever going into AF, and because endurance athletes train more frequently and tend to avoid rest the atria are chronically inflamed, which leads to fibrosis (scarring) of the atrial muscle. And of course my left atrium has been severely enlarged for decades – not as much because of sports but because I had previously had mitral regurgitation (repaired surgically 1994 but the atrium never shrunk back to normal).

But even without the mitral valve issues endurance athletes tend to have enlarged atria. And we don’t rest enough leading to inflammation and scarring. The Europace article cites several studies that link long term endurance sports with AF, compared to sedentary individuals.

Moderate exercise may actually protect against AF.

Ringo after a long run – Fremont Trail

The Europace article also cites studies that show a correlation with “occupational physical activity” and AF – meaning people that have difficult, physically demanding jobs are also in the same boat as endurance athletes.

I didn’t know this – there is also a higher rate of AF related to how tall a person is – damn! I’m 6’3” (or 6’4” – depending on what year was measured.)

The article discusses, speculates, as to the mechanism of AF in the athlete’s heart but much of this is a bit technical for this blog. Feel free to explore the article if you are curious.

The typical clinical profile of sport-related AF or atrial flutter is a middle-aged man (in his forties or fifties) who has been involved in regular endurance sport practice since his youth (soccer, cycling, jogging, and swimming), and is still active. This physical activity is his favourite leisure time activity and he is psychologically very dependent on it.

Interestingly the AF rarely occurs during running:

They almost never occur during exercise. This makes the patient reluctant to accept a relationship between the arrhythmia and sport practice, particularly since his physical condition is usually very good. The crises typically become more frequent and prolonged over the years and AF becomes persistent. Progression to permanent AF has been described by Hoogsteen et al .

The article suggests that abstinence from sports is helpful for athletes having episodes of AF, although it isn’t curative. The problem, as any endureance athletes knows, is that it is nearly impossible to get us to give up our long runs, bike rides, etc.

Other therapeutic measures are also discussed – but that is a talk that is best left to the runner and the cardiologist.

Although ablation seems to be quite effective, endurance sport cessation associated with drug therapy seems to us a more suitable approach as an initial therapy, particularly in non-professional, veteran athletes.

To conclude I’m just going to quote their conclusions right here:

Vigorous physical activity, whether related to long-term endurance sport practice or to occupational activities, seems to increase the risk for recurrent AF. The underlying mechanisms remain to be elucidated, although structural atrial changes (dilatation and fibrosis) are probably present. There is a relationship between accumulated hours of practice and AF risk. Further studies are needed to clarify whether a threshold limit for the intensity and duration of physical activity may prevent AF, without limiting the cardiovascular benefits of exercise.

I’d be interested in others opinions and experiences with these issues. Reading this article was a little emotional for me – like I said – the story checks out! I guess that if I knew what I know now I might have cut down a little on the endurance sports before I was forced to do so by permanent AF. Truly, for me, a day long run with my dog, on a trail, in a local wilderness area was the most enjoyable thing I can imagine. And at this point it isn’t even the AF preventing me from still doing it – it’s thehigh dose of beta blocker I take for rate control – really takes the wind out of my sails.

I’m not sure how much this applies to endurance athletes, but I found this interesting. As, I think, everyday knows, obesity increases the risk of cardiovascular disease, and that includes atrial fibrillation. Researchers in Sweden recently published a study where they followed 4200 obese individuals with normal sinus rhythm (ie. not in a fib at the beginning of the study) for an average of nineteen years. During that period approximately half of the subjects had had bariatric surgery – basically various surgical procedures to rearrange the internal organs to force the patient to eat less and absorb less resulting in significant, life-changing weight loss.

The study found that 12.4% in the surgery/weight loss group experienced atrial fibrillation compared to 16.8% in the non-surgical/still obese group. That’s a 29% lower rate of developing atrial fibrillation for the surgery/weight loss group. Furthermore the study also concluded that, “Compared with usual care, weight loss through bariatric surgery reduced the risk of atrial fibrillation among persons being treated for severe obesity. The risk reduction was more apparent in younger people and in those with higher blood pressure.”

Other studies have shown that weight loss can be helpful in reversing atrial fibrillation and that ablation success rate is improved with weight control. I don’t have literature citations but I read this here.

So what does this have to do with endurance athletes with A fib? All endurance athletes are already thin, right? Well, obviously that isn’t true; but probably very few endurance athletes would meet the criteria for bariatric surgery. So we should be in the low risk group to begin with – so why do so many endurance athletes end up in a fib?

Well, as everybody knows distant runners and other endurance athletes often gain weight when they have to quit or reduce exercises because of, say, atrial fibrillation. These studies suggest better outcomes with weight control regardless of method.

As to why endurance athletes have a higher rate of A fib – I’ll address that in next weeks post.

What is it? The Watchman, by Boston Scientific is a little device, sort of like a basket, that can be inserted into the left atrial appendage, theoretically blocking it off and preventing clot formation. As you probably know already, clot formation may lead to Stroke. The device was FDA approved in the US in March, 2015, and has been used in Europe since 2005.

It’s placed in the left atrial appendage via a catheter through an artery in the groin, and if all goes well the patient can discontinue their blood thinner (warfarin, etc.) within six months.

Sounds great, doesn’t it?

I know I’d love to be protected from having another TIA or stroke and not have to take a blood thinner – I’m currently on warfarin + aspirin which makes bicycling, especially mountain biking, quite hazardous. But truthfully, it’s not that I necessarily want to be off the warfarin: I just don’t want to ever have another TIA/stroke. Recall that I had my event while I was already taking Pradaxa (and I never missed a dose). I just want a treatment that is going to work.

But there is some evidence to suggest the Watchman might not be as terrific as it sounds.

A recent study showed that the risk of a major bleed over the course of three years is the same with the Watchman compared to just staying on warfarin. Huh?

Patients with atrial fibrillation (AF) who received a left atrial appendage closure device (Watchman, Boston Scientific) or stayed on long-term warfarin therapy had similar rates of major bleeding during a mean follow-up of 3.1 years, in pooled analysis of two randomized clinical trials[1]. However, patients who received the device and were able to stop taking warfarin and clopidogrel at 6 months had lower rates of major bleeding from then onward, compared with patients receiving long-term warfarin.

Furthermore, in a very thoughtful, somewhat technical, article CMS Proposal on Watchman Is the Right Decision, Dr John Mandrola, a thought leader in Cardiology and Electrophysiology, agrees with the CMS proposal that “the evidence is sufficient to determine percutaneous left atrial appendage closure therapy using an implanted device is not reasonable and necessary.”

There are two major studies in the US regarding the Watchman. According to Dr Mandrola in the PREVAIL study, “Due to an excess of ischemic strokes, Watchman did not reach noninferiority in this category in the updated analysis presented to the FDA.” In PROTECT-AF study, “ischemic strokes were numerically higher in the Watchman group.” Which, ultimately, “leads one to conclude that the device is not effective.”

As for me, personally, as much as I’d like to believe the Watchman is a solution for me, the evidence, so far, is not convincing. I’m going to wait.

By the way, if any readers have experience with the Watchman PLEASE leave a comment below. We would love to hear from you!

“The main adverse events related to this procedure are pericardial effusion, incomplete LAA closure, dislodgement of the device, blood clot formation on the device requiring prolonged oral anticoagulation, and the general risks of catheter-based techniques (such as air embolism). The left atrium anatomy can also preclude use of the device in some patients.”

By the way – I linked a couple of articles from Medscape. I’m not certain but I think you need to be registered for that sight. Sorry.

As a distance runner with atrial fibrillation, who never missed a single dose of my anti-coagulant, and who has already had a blood clot in my left atrial appendage, and has already had a “mini-stroke” – this one leaves me feeling a bit hopeless.

Feel free to read the article; but I will go over a few key points here. One of the dreaded consequences of atrial fibrillation is having a stroke. Because the top chambers of the heart, the atria (plural of atrium) are beating so fast that they are basically just sitting there vibrating, the blood pools and becomes sluggish, and is prone to forming blood clots. Combine this with an enlarged left atrium and the likelihood is even higher. The blood clot forms in a little corner of the heart called the “left atrial appendage” (LAA).

That’s where I formed a clot. If the blood clot, or a piece of the clot, breaks off it can quickly travel to the brain, get caught and cut off the circulation to part of the brain. This is a type of stroke, and is a huge problem for people with atrial fibrillation.

There are people who like to refer to a stroke as a “brain attack” because that’s what it is – like a heart attack in the brain. And like heart attacks there are big ones and small ones. I had a small one (TIA – tangent ischemia episode) that fortunately only lasted a minute or so. A big stroke, of course, can be fatal.

Important point: if a person is in atrial fibrillation and has blood clot in the LAA, it might be very stable. It might be just sitting there, hanging out, because the atria isn’t doing any beating. Everything is pretty tranquil in there. But then the person has a cardioversion (shock to reset the beating heart) or an ablation and the atrium begins to beat again, the blood starts moving through more quickly – well – now there’s a problem. Now the clot can break loose and BLAM!! – you’ve had a stroke!

The problem: it’s difficult to tell whether or not a patient has a clot prior to having a procedure. A regular echocardiogram doesn’t even show a small clot; there’s not enough detail. The best way to determine if a clot is present is to do a transesophageal echocardiogram (TEE).

Transesophageal Echocardiogram

I’ve had three TEEs – it’s not fun – sort of like swallowing a telephone. Thankfully the last two that I had involved an anesthesiologist who put me to sleep for the procedure.

As far as I know it is fairly common to have a TEE prior to having an ablation procedure; but less common before a cardioversion (the shock!), especially for people who presumably have a low risk of a LAA blot clot – like people who are appropriately anti-coagulated, or people who have had atrial fibrillation for less that 48 hours.

In this article five interesting cases are reviewed.

Case #1 – a patient who was effectively anti-coagulated but turned out to have a LAA clot anyway (sounds familiar).

Case #2 – a patient who was actually more anti-coagulated than thought necessary, and was in atrial flutter for less than 48 hours, but turned out to have a LAA clot anyway.

Case #3 – an appropriately anti-coagulated person with a low risk of clot (CHADS2 score=1), but turned out to have a LAA clot anyway.

Cases #4 and #5 were high risk patients who would be expected to have a high risk of a clot. Case #5 actually had three clots in her heart – yikes!

How does all this apply to athletes with atrial fibrillation? Well, apparently healthy, athletic patients, who are appropriately anti-coagulated, and either undergoing a planned or emergency cardioversion, still have a certain risk of having a LAA clot and subsequent stroke.

Should everybody have a TEE before having a cardioversion? Probably not. TEE is expensive, unpleasant, and if anesthesia is involved it basically takes up an entire day out of your schedule. It might be a good idea to talk it over with your cardiologist, however.

A week or so ago I re-certified in ACLS – Advanced Cardiac Life Support. ACLS is a set of emergency clinical interventions for cardiac arrest, stroke, respiratory arrest, etc., which is basically a step above BLS (Basic Life Support – formerly known as CPR). ACLS certification, in my case anyway, is done through the American Heart Association, and is only open to health care providers: doctors, nurses, dentists, advanced practice providers like PAs and nurse practitioners, EMTs, respiratory therapists, pharmacists, and so on.

I thought I’d write about it in this blog so people might know what to expect as far as the type of treatment they might experience if they have an unstable episode of atrial fibrillation.

I’m in permanent atrial fibrillation, so when I’m in one of these classes I’m glad I’m not hooked up to an EKG – I don’t feel like getting medicated or shocked!

ACLS deals with various problems using algorithms, so let’s look at the “Tachycardia with a Pulse Algorithm” which would generally apply to acute atrial fibrillation.

So basically we start with a person with a fast heart rate. Tachycardia is, by definition, a pulse over 100 beats per minute, but for ACLS purposes it generally means a pulse over 150 bpm. Obviously not all tachycardia (fast heart rate) is atrial fibrillation.

For this article I am not discussing the other types of tachycardia, even though they are in the algorithm. I assume most people reading this blog are dealing with atrial fibrillation.

The first step is to assess the patient, identify and treat any underlying cause, make sure the patient is breathing effectively, assist if necessary, and give the patient some oxygen.

Now the next step is very important – is the patient stable? Five things: 1.) Is the blood pressure too low? 2.) Is there altered mental status (confusion)? 3.) Is the patient going into shock? 4.) Chest pain? 5.) Heart failure?

Even though I am in atrial fibrillation, all the time, I don’t have any of these symptoms. But if the patient is unstable and have tachycardia, basically, they are going to be getting some electricity! That means synchronized cardioversion, and in the case of atrial fibrillation (see “narrow irregular”) that means 120-200 joules – that’s a big shock!

Notice that it says “consider sedation.” Sedation can be considered, but not if it interferes with getting the unstable patient shocked as soon as possible. If you go into unstable atrial fibrillation at a race expect that the sedation will likely be skipped and get ready to be ZAPPED.

Photo by Ted Friedman.

This is for unstable tachycardia – that means the patient is in some sort of crisis that may eventually be life threatening.

For an episode of stable atrial fibrillation expect vagal maneuvers and a referral to a cardiologist. Vagal maneuvers include firm carotid sinus massage, coughing, gagging, valsalva maneuver (holding your breath and “bearing down”), and placing your face in ice water (snow also works). A lot of people with intermittent atrial fibrillation already know how to do this.

In other words I had a “mini-stroke” and was at risk of having a full on stroke.

This TIA occurred while I was on Pradaxa, a newer, novel anticoagulant. At that point I was taken off Pradaxa, started on Lovenox (low molecular weight heparin) injections, and warfarin (Coumadin), and also aspirin. I was instructed to discontinue running, and bicycling, and limit my activity to easy walks, and a repeat TEE was scheduled two months after the initial one.

I won’t hold back any longer regarding the surprise ending – I never had a second TIA “mini-stroke” (that I know of) or stroke and the follow-up TEE (trans-esophageal echocardiogram) showed that the blood clot inside my heart is now gone. Hooray!

Photo – The little cul-de-sac is the LA appendage

Just to review how this happens: when you are in atrial fibrillation your atria is beating so fast it’s like it isn’t beating at all, just sort of vibrating. There is a part of the left atrium (the “appendage”) where the blow flow is extra sluggish, and this is where clots can form. When a tiny piece of clot breaks of and goes into the brain that’s a TIA. If a big clot is present and breaks of into the brain that’s a stroke, which of course can be disabling and even fatal.

It goes without saying that I am disappointed that this occurred while I was on Pradaxa. I figured that as long as I was taking it I was safe, and I liked not having to watch my diet or have blood tests constantly. Taking Pradaxa is easy – “set it and forget it.” Now I’m on warfarin (Coumadin), a royal pain in the butt, and have to micromanage my diet constantly – this drug is not an easy choice for a vegetarian! Eating too many greens (think kale) is dangerous as is not eating enough greens. Imagine trying to eat about the same amount of kale or broccoli or spinach each day.

Photo – vegan pizza

My target INR is between 2.0 and 3.0, but seeing as I have had a TIA while on an anticoagulant I am trying to keep it nearer to 3.0 or even higher (3.0 – 3.5).

The two months between echocardiograms was an era of angst – anxiety and fear – for me, especially the first several weeks. Every symptom, no matter how minor, seemed like stroke. For example – lie in bed trying to get to sleep and your hand becomes numb – normal, right? Not when you know you have a blood clot in your heart – that seems like a stroke! Jump up from bed, start testing the muscle strength in each arm and leg, recite the alphabet, smile, frown, move eyebrows up and down checking for asymmetry. Do you think I’m exaggerating?

Every once in a while a person stammers or mispronounces a word. Normal? Maybe, but not when you are obsessed with a gigantic blood clot lodging in your brain.

As far as exercise was concerned at first I was limiting myself to short, easy walks more appropriate for a non-athlete. Eventually I became a bit bolder and started doing longer (but slow, especially up hills) hikes of an hour or two. It took me three weeks (!) to bridge to a therapeutic INR, so I was on warfarin and Lovenox for all that time. Once I was off the injections I started doing bike rides – but they were on non-technical trails and were slow, especially while going uphill.

My brain never got the memo that I was no longer a long distance runner/cyclist so I still ate like I was, and consequently I’ve gained some weight.

At this point, after finding out the clot is no longer present, I have started increasing the intensity of my bike rides, but mostly I’m still doing bike rides. I haven’t yet started running again – but I will.

I am mountain biking again, but not on any trails that would be considered challenging. Well, that’s not 100% true, I guess.

Photo – “Adventure Without Limits?”

As far as mountain biking is concerned I am phasing out technical trails (gradually). I made a deal with my self that if I didn’t have the blood clot on the second TEE I would get a new bike – and I did. I got a Specialized AWOL, which is a “gravel grinder.” That’s sort of a cross between cyclocross bike and a loaded touring road bike – basically a bike designed for gravel or dirt roads – we have an infinite supply of these around here so I have a lot of exploring ahead of me.

As far as that blood clot is concerned I’m very pleased it has gone away – but I am not fooling myself that it is gone forever. It could return at any time. It wasn’t there when I had my second TEE, but it could actually be there right now – how would I know? How long had it been there and how many times have I had a clot in that area? There’s no telling without doing a ridiculously expensive, somewhat invasive test over and over. I guess all I can do is stay vigilant, take my meds, watch the diet, and keep on trying to run, hike, and ride, even if it is at a reduced level.